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Properties of the Arterial Wall
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
When the PWV is measured from the mean apparent phase velocities, this value is derived from the whole wave and will only be affected by the mean blood flow velocity, which is less than 5.0 percent of the PWV. Such values are shown at various mean arterial pressures in Figure 4.11. These velocities were measured in the ascending aorta of the dog (Nichols and McDonald, 1972). It can be seen that the velocity remains unchanged at about 4.0 m/s from a mean pressure of 60–110 mmHg. A comparable set of values is shown that were measured during continuous intravenous infusion of norepinephrine. The wave velocity is virtually unchanged up to a pressure of 100 mmHg, but thereafter there is an appreciable increase in PWV, presumably attributable to the fact that contraction of smooth muscle cells in peripheral arteries increases aortic pressure and transfers stress from elastin to collagen, which causes stiffening of the aortic wall. This dependence of PWV on arterial blood pressure was also observed by Pruett et al. (1988).
Cardiac Hypertrophy, Heart Failure and Cardiomyopathy
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
This is a cardiac syndrome characterized by transient LV dysfunction with apical ballooning, electrocardiographic changes that can mimic acute myocardial infarction, and release of myocardial enzymes in the absence of obstructive coronary artery disease. This syndrome was first described in 1991 in Japan and named Takotsubo which is a pot with a round bottom and narrow neck used for trapping octopuses in Japan. It has also been called LV apical ballooning syndrome or stress cardiomyopathy. It has now been reported throughout the world. It particularly occurs in post-menopausal women. Symptoms are often preceded by emotional or physical stress. Norepinephrine concentration is elevated in most patients. Takotsubo cardiomyopathy has a favourable prognosis with a low mortality and a complete recovery of the contractile function in nearly all cases. Rare fatal cases describe contraction band necrosis within myocytes at autopsy at the apex of the left ventricle.32 The same kind of reversible myocardial dysfunction is occasionally encountered in patients with intracranial haemorrhage or other acute cerebral accidents (neurogenic myocardial stunning).33 Takotsubo cardiomyopathy is impossible to define at autopsy unless there has been clinical evidence during life and pathologically there is localized evidence of ischaemia such as contraction band necrosis or localized acute infarction.
Inhalational Durg Abuse
Published in Jacob Loke, Pathophysiology and Treatment of Inhalation Injuries, 2020
Jacob Loke, Richard Rowley, Herbert D. Kleber, Peter Jatlow
Cocaine alters the interneural communications of neurotransmitters—catecholamines, norepinephrine, and dopamine (Ritchie and Green, 1980)—resulting in an excess of norepinephrine and dopamine, and blockade of serotonin synthesis. Norepinephrine release leads to stimulation of the sympathetic nervous system, hypothalamus, and the reticular-activating system, accounting for the sympathomimetic effects, the effects on thirst, hunger, body temperature, emotions, arousal, and sleep. Receptor supersensitivity (beta-adrenergic or dopaminergic) may be a neurochemical substrate for postcocaine dysphoria or craving, and human cocaine abusers have been noted to have elevated levels of plasma growth hormone and decreased plasma prolactin, which confirms the adrenergic and dopaminergic receptor effects seen in animals (Kleber and Gawin, 1984a,b). The alteration in dopaminergic receptors and the dopaminergic reward pathway may have pharmacologic implications for the treatment of the craving that often leads to cocaine relapse.
Comparison of ultrasound-based measures of inferior vena cava and internal jugular vein for prediction of hypotension during induction of general anesthesia
Published in Egyptian Journal of Anaesthesia, 2023
Dalia Khaled, Ismail Fathy, Yasser M. Elhalafawy, Dina Zakaria, Islam Rasmy
Mean blood pressure was measured with the patient lying in supine position in either upper limb beginning from the baseline preoperative reading till skin incision at 1-minute intervals, taking in consideration that the maximum duration for recording the readings of the blood pressure is 15 minutes because if hypotension occurred after this duration it is unlikely to be due to the effect of induction of anesthesia. Heart rate recorded beginning from the baseline pre-operative reading at 1-minute intervals until 15 minutes after anesthetics administration or until skin incision whichever is earlier. Norepinephrine consumption was calculated for each patient. Demographic data: (age – gender – comorbidities – current medications) were routinely collected. Also incidence of prolonged post-induction hypotension, incidence of severe post-induction hypotension and incidence of bradycardia were determined.
Prehospital Ultrasound Diagnosis of Massive Pulmonary Embolism by Non-Physicians: A Case Series
Published in Prehospital Emergency Care, 2023
Aaron E. Robinson, Nicholas S. Simpson, John L. Hick, Johanna C. Moore, Gregg A. Jones, Michael D. Fischer, Seth Z. Bravinder, Kolby L. Kolbet, Robert F. Reardon
A 59-year-old female complained to a family member about shortness of breath and then collapsed. She was found by local EMS with an altered level of consciousness and shortly after their arrival on scene, she suffered a pulseless electrical activity (PEA) arrest. The patient was intubated at the originating hospital and achieved return of spontaneous circulation. The resuscitation was complicated by ongoing hypotension with systolic pressures in the 80 s and hypoxemia with oxygen saturations in mid-80s on 100% oxygen. Norepinephrine was started to support blood pressure. The patient was deemed too unstable for local care and a helicopter was requested. Electrocardiogram demonstrated sinus tachycardia without clear ischemia. Chest radiograph was unremarkable. The helicopter crew, staffed by a critical care paramedic and a critical care nurse, arrived and performed a bedside ultrasound. The RUSH exam identified a very large right ventricle with septal bowing and limited left ventricular filling. These findings were communicated to the treating physician at the referring hospital. Alteplase was immediately started at the referring facility based on the POCUS findings alone, without computed tomography (CT) confirmation. The patient was transferred to the tertiary care facility with improving vasopressor requirements. She underwent CT pulmonary angiography, which demonstrated multiple segmental pulmonary emboli. She was discharged home neurologically intact.
The current and future status of inotropes in heart failure management
Published in Expert Review of Cardiovascular Therapy, 2023
Angelos Arfaras-Melainis, Ioannis Ventoulis, Effie Polyzogopoulou, Antonios Boultadakis, John Parissis
Norepinephrine is a naturally occurring molecule that exerts its effects by binding to alpha-1 adrenergic receptors in the vasculature. Through this mechanism, it results in vasoconstriction and thus raises mean arterial pressure via increasing both systolic and diastolic blood pressures. Additionally, norepinephrine acts on cardiac beta-1 receptors, thereby increasing cardiac contractility and chronotropy [8]. In the setting of acute HF and cardiogenic shock, norepinephrine is most commonly used in conjunction with other inotropic agents and inodilators to counteract their potential hypotensive effects [9]. Norepinephrine is also widely utilized in the management of other shock etiologies, including septic shock [43]. In clinical practice, norepinephrine is titrated to the desired blood pressure, typically infused at a rate ranging from 0.01 to 0.03 μg/kg/min, with doses up to 1 μg/kg/min used in certain cases. Despite its therapeutic benefits, norepinephrine has the potential to cause adverse events such as tachycardia, hypertension, and tachyarrhythmias [7,8]. Furthermore, norepinephrine has been reported to induce a toxic effect on cardiomyocytes, primarily due to beta-adrenergic stimulation-induced apoptosis [44].